As a pathogenic mechanism in periodontal disease, the complement system may play an important modulating role. Two aspects of the complement system will be examined. In the first, the observation that C3 cleavage products influence lymphocyte proliferation in response to antigens by interfering with monocyte-lymphocyte interactions will be further studied. The effects of these cleavage products on mediator (monokine) production by monocytes and lymphokine production by T and B lymphocytes will also be examined. Secondly, the role of antibody in the activation of the alternative pathway of complement (APC) will be studied. Preliminary data indicate that "natural antibody" to zymosan, an APC activator, enhances activation. Such antibody appears to be of the IgG class. We propose to define the mechanism of action of antibody in the APC, and to examine the roles of the Fab and Fc portions of the IgG molecules in this phenomenon.